RESUMEN
The relationship between cerebral rhythms and early sensorimotor development is not clear. In recent decades, evidence revealed a rhythmic modulation involving sensorimotor processing. A widely corroborated functional role of oscillatory activity is to coordinate the information flow across sensorimotor networks. Their activity is coordinated by event-related synchronisation and desynchronisation in different sensorimotor rhythms, which indicate parallel processes may be occurring in the neuronal network during movement. To date, the dynamics of these brain oscillations and early sensorimotor development are unexplored. Our study investigates the relationship between the cerebral rhythms using EEG and a typical rhythmic movement of infants, the non-nutritive sucking (NNS) behaviour. NNS is an endogenous behaviour that originates from the suck central pattern generator in the brainstem. We find, in 17 infants, that sucking frequency correlates with beta synchronisation within the sensorimotor area in two phases: one strongly anticipating (~3 s) and the other encompassing the start of the motion. These findings suggest that a beta synchronisation of the sensorimotor cortex may influence the sensorimotor dynamics of NNS activity. Our results reveal the importance of rapid brain oscillations in infants and the role of beta synchronisation and their possible role in the communication between cortical and deep generators.
RESUMEN
Encephalopathy with status epilepticus during sleep (ESES) is an epileptic encephalopathy, as defined by the International League Against Epilepsy (ILAE) Task Force on Classification and Terminology, that is, a condition in which the epileptic processes themselves are believed to contribute to the disturbance in cerebral function. Clinical manifestations of ESES are heterogeneous: apart from different seizure types, they consist in combinations of cognitive, motor, and behavioural disturbances associated with a peculiar electroencephalographic pattern of paroxysmal activity significantly activated during slow sleep, which culminates in a picture of continuous spikes and waves during sleep (CSWS). The pathophysiological mechanisms underlying this condition are still incompletely understood. Establishing a clear-cut correlation between EEG abnormalities and clinical data, though interesting, is very complex. Computer-assisted EEG analyses especially if combined with functional magnetic resonance imaging (EEG-fMRI) and metabolic neuroimaging have recently emerged as useful approaches to better understand the pathophysiological processes underlying ESES. Treatment of ESES is not just limited to seizures control but it should be focused on controlling neuropsychological outcome through an improvement of the continuous epileptiform activity. General agreement on treatment guidelines is still lacking. Implementation of new techniques might allow a better understanding of the pathophysiology of ESES and could enhance therapeutics options.
RESUMEN
PURPOSE: To study clinical, EEG, neuropsychological and behavioural evolution of three patients presenting with epileptic activity triggered by eye closure (EC) over a mean 10-year follow-up period. METHODS: All patients were studied at the time of the first observation (T0) and after a long follow-up period (T1). At both T0 and T1, each patient underwent: 1) traditional and specific activation techniques during prolonged video-EEG monitoring to detect possible inducing factors; 2) neuropsychological evaluations during video-EEG monitoring either with eyes closed or eyes open to detect any transient cognitive impairment (TCI); 3) detailed neuropsychological assessment without simultaneous EEG recording, to detect any stable cognitive impairment (SCI). RESULTS: EEG recordings showed transient, generalized paroxysms in one case and a continuous epileptic activity triggered by eye closure in the other two cases, at both T0 and T1. In all patients, no particular epileptiform discharge-induced factors were identified except for eye blinking (spontaneous, voluntary or induced by corneal reflex). The results of neuropsychological assessment while eyes were closed as compared to performances with eyes open, showed no significant differences at T0 or at T1 in two cases, thus possibly indicating the absence of TCI. Wechsler Intelligence Scales showed a decrease in performance at T1 in the two patients with eye closure-induced, continuous epileptiform activity. Detailed neuropsychological assessment without EEG recordings demonstrated an impairment of facial recognition ability in all three patients at T1. CONCLUSIONS: The lack of any differences between the results of neuropsychological tests performed with eyes open and eyes closed in two patients might suggest that not all eye-closure-triggered paroxysms are associated with TCI. On the other hand, our data highlight that EC-triggered, EEG epileptic discharges can produce long-lasting neuropsychological and behavioural effects, and also indicate that EEG discharges recurring over time might exert a disruptive effect on cognitive functions. Our three patients showed extreme variability across the neuropsychological tasks except for a facial recognition deficit that was evident in all cases, thus suggesting a possible dysfunction of temporo-occipital brain structures and/or of the fusiform face area as recently demonstrated by combined fMRI/EEG studies in patients with fixation-off sensitivity.